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Scott P. Sherry, MS, PA-C, FCCM

Assistant Professor

Department of Surgery

Division of Trauma, Critical Care and Acute Care Surgery

Traumatic Brain Injuries

DISCLOSURES

– Nothing to disclose

– Discussion of off

label medication use

Objectives

• Overview of the cerebral anatomy

• Description of the epidemiology of TBI

• Understand and describe different types of TBI

• Understand and describe management strategies

of patients with suspected or known traumatic

brain injury including intercranial hypertension

• Understand “prognosis” in the TBI patient

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Meningeal Anatomy Review

•

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Traumatic Brain Injury

• 500,000 cases each year in the US

• 10% die before reaching medical care

• Severity:

• 80% mild

• 10% moderate

• 10% severe

• Broad injury pattern

– Concussion, DAI, SAH, SDH, IPH, IVH, EDH

Head Injury Epidemiology

• Trauma mortality: 40 % secondary to brain

injury

• Overall mortality: 7 - 36 % (head injury alone)

• Annual mortality: 100,000

Head Injury Disability

• Survivors of TBI and permanent disability:

• 10 % of those with a mild injury

• 66 % of those with a moderate injury

• ~100 % of those with a severe injury

• 90,000 newly disabled per year

• For those who survive gunshot wounds:

• 10 % have severe disabilities

• 20 % have moderate disabilities

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Traumatic SAH

• Scattered appearance

• Has a risk of vasospasm

– Less incidence than aneurysmal SAH

Pedestrian Struck: SDH, SAH

Fall from Car: IPH, SDH, SAH

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Epidural Hematoma

• Usually an arterial injury

• Has a “classic presentation”

– DO NOT MISS THIS

• Lens shaped appearance to lesion

– Suture attachments

• Urgent surgical intervention is warranted

• Temporal bone fx with middle menigeal artery

• Generally good recovery with prompt intervention

Epidural Hemorrhage

Epidural Hemorrhage

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Epidural Hemorrhage

Epidural Hemorrhage

Epidural Hemorrhage

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Epidural Hemorrhage

Epidural Hemorrhage

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Subdural Hematoma

• Venous injury generally

– Bridging Veins

• Crescent shaped lesion

• Follows subdural tact

– Has attachment points at the front / back.

• Some are acute, chronic and acute on chronic

bleeds

• Most common traumatic mass effect lesion

Subdural Hematoma

Subdural Hematoma

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Subdural Hematoma

Subdural Hematoma

Subdural Hematoma

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Subdural Hematoma

Subdural Hematoma

Subdural Hematoma

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Subdural Hematoma

Subdural Hematoma

Subdural Hematoma

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Subdural Hematoma

Subdural Hematoma

Subdural Hematoma

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Motor Vehicle Crash: SDH

Unwitnessed Fall: SDH

Fall from Barstool: IPH, SDH

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Pedestrian Struck: IPH, SDH

Diffuse Axonal Injury

• Active process triggered by the injury that

takes about 24 hours

• Frequently without radiographic abnormality

• Frequently seen in areas of radiographically

apparent “shear injury”

– this latter finding usually occurs at the grey-white

junction

– MRI is diagnostic

• Major cause of long-term disability

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MVC: IPH, DAI, IVH, SAH

Thalamic Bleed

Cerebral Edema

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MVC: IPH, DAI, IVH, SAH

Assault: IPH

PedestrianStruck: IPH

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ATV Crash: Skull Fx, ICH

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“Found Down”

Suspected Fall

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“Found Down”

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head

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GSW Head

GSW Head

GSW Head (BONE)

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GSW Head (BONE)

GSW Head (BONE)

GSW Head (BONE)

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GSW Head (BONE)

GSW Head (BONE)

GSW Head (BONE)

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GSW Head (BONE)

GSW Head (BONE)

GSW Head (BONE)

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GSW Head (BONE)

GSW Head (BONE)

GSW Head (BONE)

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GSW Head (BONE)

GSW Head (BONE)

Shot Gun Wounds

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Prehospital Care

• High index of suspicion

• Trauma Center Transport

– Immediate

• Prevention of secondary insults

– Hypoxia / Hypotension

Hospital Care

• Immediate CT

– Any LOC

– Amnesia to event

• If e/o TBI

– Neurosurgical Consult

– Prompt transfer if needed

– Frequent neuro checks

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PREVENT Secondary Injury

• Hypoxia and hypotension

– 2 major causes of secondary CNS injury following

head trauma

– These complications occur frequently

• Prevention could have the greatest effect of

any currently available treatment for head

trauma

Outcome from Severe Brain Injury

• Univariate predictors of poor outcome:

– ICP > 25 mm Hg

– MAP < 70 mm Hg or

– CPP < 60 mm Hg and fluid balance < -594 mL

Clifton et al. Crit Care Med 2002;30:739–745.

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Increased Intracranial Pressure

• Monroe Kellie

– Volume of the skull is a constant

• Brain ~ 85%

• Blood ~5%

• CSF ~ 10%

• An increase in the volume of any of these will

raise ICP

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Important Formulas

• Cerebral Perfusion Pressure (CPP)

= Mean Arterial Pressure – Intercranial Pressure

– Goal CPP > ~ 60

– Guidelines = 50-70mm Hg

Increased Intracranial Pressure

• Management

– Correct the underlying pathophysiology if possible

– Airway control and prevention of hypercapnea are crucial

• Posture and head position

– ICP monitoring

– Avoid jugular vein compression

• Head in neutral position with body

• Head of bed elevated > 30 deg

• Cervical collars loose or remove

• No circumferential ETT Tape

Increased Intracranial Pressure

• Hyperventilation (PaCO2 < 35 mmHg)

• Works by decreasing blood flow

– should be reserved for emergency treatment and

only for brief periods.

• Avoid Severe Hyperventilation < 30

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Increased Intracranial Pressure

• Pharmacologic options

– Mannitol 1G / KG

– Follow up doses

• 0.25-0.5 gm/kg q4h

• Follow Serum OSM < 320

– Hypertonic Saline

• 3%

• 7.5%

• 23.4%

– Lasix / Diuretics

Increased Intracranial Pressure

• Sedation and Analgesia

– Opiods

– Benzodiazepines

– Propofol

• Decrease cerebral metabolic rate, which is coupled to blood flow

– Prevent hyperthermia

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Slide 118

Increased Intracranial Pressure

• Neuromuscular junction blockade

– Titrate with train-of-four stimulator to 1 or 2

twitches

• High-dose barbiturates

– E.g., pentobarbital 5 – 12 mg/kg load followed by

infusion to control ICP

– Risk of infection

Slide 119

Increased Intracranial Pressure

Surgical options

• Resect mass lesions if possible

• Ventriculostomy Drainage

• Craniectomy

– Lateral for focal lesions

– Bifrontal (Kjellberg) for diffuse swelling

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CCM April 2013

Recovery - Trajectory

• Emergence of conscious awareness

• Recovery of higher processing

• Return of functional capacity

Recovery from COMA

• Vegetative state

• Minimally conscious state

• Emergence from minimally conscious state

– Functional communication

– Object use

• Time course variable

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Natural History of VS / MCS

• Not well studied

– 50% MCS / 3% VS had no or mod disabilities when

evaluated after 1 year of injury

– More rapid improvement in the traumatically

injured

• After recovery of awareness

– May have significant neurologic impairments

– Motor, dystonic, movement disorders, aphasia.

– Attention, mood, memory, seizure disorders

Organ Donation

• Treat all traumatic brain injuries to the fullest

extent

• Potential for good outcomes is unknown

• Good prehospital care = good outcomes

• Good prehospital care with bad outcomes can

lead to good outcomes for others

– Organ donation

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Summary

• Recognize life threatening neurological

problems early and have a high degree of

suspicion

• Intubate for GCS < 8

• Treat ICP elevations > 20 aggressively

• Prevention is KEY

– You can’t get back what you loose